Sem 2 Medical Emergencies Dental Office

7/30/2019 Sem 2 Medical Emergencies Dental Office

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INTRODUCTION

PREVENTION

PREPARATION

CLASSIFICATION OF LIFE THREATENING EMERGENCIES

UNCONSCIOUSNESS

› Vasodepressor Syncope› Postural Hypertension

› Acute Adrenal Insufficiency

RESPIRATORY DISTRESS

› Foreign Body Airway Obstruction

› Hyperventilation

›

Asthma› Heart Failure and Acute Pulmonary Edema

ALTERED CONSCIOUSNESS

› Diabetes Mellitus: Hyperglycemia and Hypoglycemia

› Thyroid Gland Dysfunction

› Cerebro vascular Accident

SEIZURES

DRUG RELATED EMERGENCIES

› Drug Overdose Reactions

› Allergy

CHEST PAIN

› Angina Pectoris

› Acute Myocardial Infarction



Goldberger 1990, “When you prepare foran emergency, the emergency ceases

to exist.”



Goals of physical evaluationPhysical evaluation –

Medical history questionnaire,

Physical examination

Dialogue history.



Class1: Healthy patient with no systemic disease.

Class 2: Mild Systemic disease with no limits on activity.

Class 3: Severe systemic disease that limits activity. Class 4: Incapacitating systemic disease that is life

threatening.

Class 5: Moribund and E refers to emergency of any kind.



Recognize patient‟s anxiety level.

Consider using pre-medication or sedation

Schedule morning appointments.

Minimize waiting time and watch appointment length. Make sure to use adequate pain control. This will vary from

patient to patient.

Monitor vital signs.

Medical consult if required.



Drug Recommended dosage for adults Alprazolam 4 mg / day Diazepam 2-10 mg

Flurazepam 15-30 mg Midazolam

Rarely used

Oxazepam 10-30 mg Triazolam 125-250µg

Eszopiclone 2-3 mg Zaleplon 5-10 mg Zolpidem 10 mg



Situation Agent Regimen

Standard general

prophylaxis Amoxicillin Adults: 2g Children: 50mg/kg orally 1 hour before the procedure Inability to take oral

medications Ampicillin Adults: 2g Children: 50 mg/kg IM/IV 30 min before procedure

Allergy to penicillin Clindamycin or Cephalexin/Cefadroxil or Azithromycin/

Clarithromycin

Adults 600 mg Children 20 mg /kg Adults 2g Children 50mg/kg Adults 500 mg Children 50 mg/kg Orally 1 hour before the procedure

Allergy to penicillin and

inability to take oral

medications Clindamycin or

Cefazolin

Adults 600mg Children 20mg/kg IV 30 min before Adults 1g Children 25 mg/kg IM/IV 30 min before



Endocarditis prophylaxis RECOMMENDED:

High-risk category-

Prosthetic cardiac valves- bioprosthetic and homograft

valves

Previous bacterial endocarditis

Cyanotic congenital heart disease- e.g., single ventriclestates, trans position of great arteries, tetralogy of fallot

Surgically constructed systemic pulmonary shunts

Moderate-risk category-

Other congenital cardiac malformations

Acquired valvular dysfunction- e.g., rheumatic heartdisease

Hypertrophic cardiac myopathy Mitral valve prolapse with valvar regurgitation or

thickened leaflets



Endocarditis prophylaxis NOT RECOMMENDED:

Negligible-risk category-

Isolated atrial septal defect (ASD)

Surgical repair of ASD, VSD or patent ductus arteriosus(no residual effects in 6 months)

Previous coronary artery bypass graft surgery

Mitral valve prolapse with out valvular regurgitation

Physiologic, functional or innocent heart murmurs Previous rheumatic fever without valvular dysfunction

Cardiac pacemakers and implanted defibrillators



Module one – critical or essential emergency drugs

Category Generic drug alternative quantity Availability Allergy –

anaphylaxis Epinephrine None 1 preloaded

syringe +3x1ml ampules

1:1000

(1mg/ml) allergy –

histamine

blocker Chlorphenira

mine Diphenhydra

mine

(Benadryl) 3x1 ml

ampules 10 mg/ml

Oxygen Oxygen 1 “E” cylinder Vasodilator Nitroglycerin Nitrostat

sublingual

tablets 1 metered spray

bottle 0.4 mg /metered

dose Bronchodilator Albuterol Metaproterenol 1 metered dose

inhaler Metered aerosol

inhaler Antihypoglyce

mic Sugar Insta – glucose

gel 1 bottle Inhibitor of

platelet

aggregation Asprin None 2 packets 325mg/tablet



Equipment Recommended Alternative Quantity Oxygen delivery

system Positive pressure and

demand valve

Pocket mask Oxygen delivery

system with bag valvemask device Minimum: 1 large

adult, 1 child

1 per employee Automated electronic

defibrillator(AED)

Many 1 AED Syringes for drug

administration Plastic disposable

syringes with needles 3x2 ml syringes with

needles for parenteraldrug administration Suction and suction

tips High volume suction Large diameter, round

ended suction tips Non electrical suction

system Office suction system Minimum 2

Tourniquets Robber and Velcrotourniquet; rubber

tubing spygmomanometer 3 torniquets and 1

spygmomanometer Magill intubation

forceps Magill intubation

forceps 1 pediatric Magill

intubation forceps



Module two – secondary/ noncritical drugs and equipment

Category Generic Drug Alternative Quantity Availability Anticonvulsant Midazolam diazepam 1x5 ml vial 5 mg/ml Analgesic Morphine

sulphate Meperidine 3x1 ml ampules 10 mg/ml Vasopressor Phenylephrine 3x1 ml ampules 10 mg/ml Antihypoglycem

ic 50% dextrose Glucagon 1 vial 50 ml ampule Corticosteroid Hydrocortisone

sodium succinate Dexamethasone 2x2 ml mix- o – vial 50 mg/ml

Antihypertensive Esmolol Propranolol 2x100 mg/ml

vial 100 mg/ml Anticholinergic Atropine Scopolamine 3x1 ml ampules 0.5 mg/ml

Respiratory

stimulant Aromatic

ammonia 2 boxes 0.3 ml/vaporole

Antihypertensive Nifedipine 1 bottle 10mg/capsule



Module three – Advanced Cardiac Life Support (ACLS) : essentialdrugs

Category Generic Drug Alternative Quantity Availability Cardiac Arrest epinephrine 3x10 ml

preloaded

syringes 1:10,000

(1mg/10ml

syringe) Analgesic Morphine

sulphate N2O – O2 3x1 ml ampules 10 mg/ml

Antidysrhythmic Lidocaine Procainamide 1 preloaded

syringe and 2x5

ml ampules 100 mg/ syringe

Symptomatic

Bradycardia Atropine Isoproterenol 2x10 ml

syringes 1.0 mg/10 ml ParoxysmalSupraventricular

Tachycardia verapamil 2x4 ml ampules 2.5 mg/ml



Module four – antidotal drugs

Category Generic Drug Alternative Quantity Availability Opioid

antagonist Naloxone nalbuphine 2x1 ml ampules 0.4 mg/ml Benzodiazepine

antagonist Flumazenil 1x 10 ml vial 0.1 mg/ml

Anticholinergic

toxicity Antiemergence

delirium

Physostigmine 3x2 ml ampules 1 mg/ml



Syncope is a general term referring to a sudden, transient loss ofconsciousness that usually occurs secondary to a period of

cerebral ischemia.Predisposing factors:

Psychogenic factors

Fright

Anxiety Emotional stress

Receipt of unwelcome news

Pain especially sudden &unexpected

Sight of blood/ surgical/ dental instruments

(e.g. local anesthetic syringe)



Non psychogenic factors

Erect sitting or standing posture

Hunger from dieting or a missed meal

Exhaustion

Poor physical condition Hot, humid, crowded environment

Male gender

Age between 16 and 35 years



Prevention: Proper positioning and Anxiety relief

Pre-syncope

Warm feeling in face and neck.

Pale or ashen coloration.

Sweating.

Feels cold.

Abdominal discomfort. Lightheaded or dizziness.

Mydriasis (Pupillary dilatation.)

Yawning.

Increased heart rate.

Steady or slight decrease in blood pressure.



Syncope

Patient loses consciousness.

Generalized muscle relaxation. Bradycardia (Weak thready pulse.)

Seizure (Twitching of hands, legs, and face.)

Eyes open (Out and up gaze.)

Post-syncope

Variable period on mental confusion.

Heart rate increases (Strong rate and rhythm.)

Blood pressure back to normal levels.



Pathophysiology: Stress

Catecholamines release

Decreased peripheral vascular resistance & ↑ blood flow to peripheralmuscles

↓ venous return

↓ circulatory blood vol. & drop in arterial B.P.

Activation of Compensatory mechanisms

Reflux bradycardia develops (< 50)

Significant drop in cardiac output associated with fall in B.P below thecritical level

Cerebral ischemia & loss of consciousness



Assess consciousness (loss of response to sensory stimulation)

Activate office emergency system

P- Position patient supine with feet elevated slightly

A→B→C – Assess & open airway (head tilt &chin lift); assess airway patency&breathing; assess circulation (palpation of carotid pulse)

D – Definitive care:

Administer O2

Monitor vital signs

Perform additional procedures:

Administer aromatic ammonia vaporole

Administer atropine if bradycardia persists

Do not panic!

Post syncopal recovery- delayed recovery- Postpone dental treatment Activate EMS

Determine precipitating factors



Predisposing factors:

Administration and ingestion of drugs e.g. antihypertensiveslike sodium depleting diuretics, calcium channel blockers&ganglion blocking agents, sedatives and narcotics,histamine blockers, levo dopa

Prolonged period of recumbency or convalescence

Inadequate postural reflex Late stage pregnancy

Advanced age

Venous defects in legs (e.g. varicose veins)

Recovery from sympathectomy

Addisson‟s disease

Physical exhaustion and starvation

Chronic postural hypotension (Shy – Drager syndrome)



Clinical manifestations:

Precipitous drops in blood pressure and lose consciousnesswhenever they stand or sit upright

Do not exhibit any prodromal signs and symptoms

May become lightheaded, or develop blurred vision

Clinical signs and symptoms - precipitating drugs Blood pressure during syncopal period is quite low

Un like vasodepressor syncope , heart rate during posturalhypotension remain at the baseline level or somewhat higher

Consciousness returns rapidly once the patient is returned to

the supine position



Pathophysiology: When patient moves into an upright position

SBP drops and approaches 60 mm Hg in one minute

DBP also drops

Slight changes in heart rate and not at all

Cerebral blood flow drops below the critical level

May lose consciousness

Once the patient is placed into supine position, reestablishment of

cerebral blood flow occurs



P- Position patient supine with feet elevated slightly

A→B→C – Assess & open airway (head tilt &chin lift); assess

airway patency& breathing; assess circulation (palpation ofcarotid pulse)


Administer O2

Monitor vital signs

Patient recovers consciousness-

slowly reposition chair delayed recovery -

activate EMS

Continue BLS as needed and discharge patient



A third potentially life - threatening situation that may result in theloss of consciousness. The condition is uncommon, ispotentially life – threatening, but is readily treatable.


Lack of gluco-corticosteroid hormones

Mechanism 1: sudden withdrawal of steroid hormones in thepatient who suffers primary adrenal insufficiency (Addison’sdisease)

Mechanism 2: After the sudden withdrawal of steroidhormones from a patient with normal adrenal cortices but

with a temporary insufficiency resulting from corticalsuppression through prolonged exogenous gluco-corticosteroid administration (secondary insufficiency)

Mechanism 3: Stress either physiologic or psychological.



If the adrenal gland cannot meet the increased demand, clinicalsigns and symptoms of adrenal insufficiency develop.

Mechanism 4: After bilateral adrenalectomy

Mechanism 5: After sudden destruction of pituitary gland.

Mechanism 6: Injury to the both adrenal glands (trauma,infection, thrombosis, or tumor)

Prevention:

History of rheumatic fever, asthma, TB, emphysema, other lung diseases, arthritis and rheumatism

Allergic history to drugs, food, medications, latex

Dialogue history

Rule of TWOs

In a dose of 20 mg or more of cortisone or its equivalent

Via oral or parenteral route for a continuous period of twoweeks or longer

Within 2 years of dental therapy



Dental therapy considerations:

Glucocorticosteroid coverage

Stress reduction protocol

Clinical manifestations: Symptom Sign Laboratory finding 1. Weakness, tiredness,

fatigue 2. Anorexia 3. GI symptoms like

nausea vomiting

constipation,

abdominal pain,

diarrhea 4. Salt craving 5. Postural dizziness 6. Muscle or joint pain

1. Weight loss 2. Hyperpigmentation 3. Hypotension (<110

mm Hg systolic 4. Vitiligo

5. Auricular

calcification

1. Electrolyte

disturbance:

Hyponatremia Hyperkalemia Hypercalcemia 1. Azotemia 2. Anemia 3. Eosinophilia



Pathophysiology



Management :

Conscious

Terminate dental treatment

P – Position patient comfortably if asymptomatic;

Supine with legs elevated slightly, if symptomatic

A→B→C – Assess & open airway (head tilt &chin lift); assess airwaypatency& breathing; assess circulation (palpation of carotid pulse)


Monitor vital signs

Summon medical assistance

Obtain emergency kit and O2

Administer glucocorticosteroid



Prevention:



General Signs and Symptoms

Gasping for breath

Patient grabs at throat

Panic

Suprasternal or supraclavicular retraction Inability to speak, breathe, cough

If Partial Obstruction

Snoring Gurgling

Wheezing

„Crowing‟ sound on inspiration

Forceful cough

Wheezing between cough

Absent or altered voice sounds Possible cyanosis, lethargy, disorientation

If Total Obstruction - No noise



Visible objects – if assistant is present

Place patient into supine or Trendelenburg position

Use Magill intubation forceps or suction

if assistant is not present

Instruct patient to bend over arm of chair with their head down

Encourage patient to cough

Aspirated foreign bodies

Place patient in left lateral decubitus position

Encourage patient to cough



CONSCIOUS victim with obstructed airway

Identify complete airway obstruction Ask – „Are you choking‟

Apply abdominal thrusts until foreign body is expelled

Have medical or paramedical personnel to evaluate the patient



CONSCIOUS victim with known obstructed airway who losesconsciousness

Place victim in supine position with head in neutral position

Maintain airway (head tilt – chin lift)

Look in mouth for foreign object prior to ventilation.

If INEFFECTIVE:

Perform abdominal thrust, repeating until the object is

expelled

Check for foreign body. If visible, perform finger swipe toremove



Establishing an emergency airway –

Non invasive procedures

Invasive procedures



If foreign body is not retrieved

Consult radiologist

Obtain appropriate radiographs and initiate medical

consultation

Perform bronchoscopy to visualize and retrieve foreign body



It is defined as ventilation in excess of that required tomaintain normal blood pa O2 (arterial oxygen tension) andpa CO2 (arterial carbon dioxide tension). It is produced by increase in frequency or depth of respiration, or both.

Common emergency occur in dental office , almost always

occur is a result of extreme anxiety.Prevention:

Through prompt recognition and management of anxiety

Physical evaluation of the patient

The vital signs of apprehensive patients may deviate fromnormal. Recording the vital signs at the patient‟s initial visit

Stress reduction protocol is the primary means of preventinghyperventilation




system Signs and symptoms cardiovascular Palpitations

Tachycardia Precordial”pain”

Neurologic Dizziness Lightheadedness

Disturbance of consciousness Disturbance of vision

Numbness and tingling of

extremities Tetany (rare)

Respiratory Shortness of breath Chest “pain”

Dryness of mouth Gastro intestinal Globus hystericus (subjective

feeling of a lump in the throat) Epigastric pain

Musculoskeletal Muscle pain and cramps Tremor

Stiffness Carpopedal tetany

Psychological Tension Anxiety and nightmares



Pathophysiology:

Anxiety

Increased rate and depth of respiration

↑ exchange of O2 & CO2 by lungs

↑ blowing off of CO2and paCO

2decreases

Hypocapnia

↑ in blood pH

Respiratory alkalosis



Hypocapnia → vasoconstriction of cerebral vessels →

cerebral ischemia

Respiratory alkalosis → ↓ ionized calcium



Management:

Recognize problem (rapid , deep, uncontrolled breathing)

P – Position patient comfortably usually upright

A → B → C – Basic life support as needed


Remove dental materials from patient‟s mouth

Calm patient

Correct respiratory alkalosis – instructed to breathe 7% CO2 &93% O2

or to rebreathe the exhaled air

Initial drug management – Benzodiazepines

Dental care may continue if both doctor and patient agree

Discharge patient



In 1830 Eberle, a Philadelphia physician, defined it as“paroxysmal affection of the respiratory organs,characterized by great difficulty of breathing, tightness

across breast, and a sense of impending suffocation, withoutfever or local inflammation.”

Today it is defined as “a chronic inflammatory disorder that ischaracterized by reversible obstruction of the airways.”




Extrinsic or allergic asthma,

The allergens may be airborne – house dust, feathers, animaldander, furniture stuffing, fungal spores, or plant pollens.

Food and drugs – cow‟s milk, egg, fish, chocolate, shellfish,tomatoes, penicillins, vaccines , asprin, and sulfites.

Type I hypersensitivity reaction – Ig E antibodies produced inresponse to allergen

Approximately, 50% asthmatic children becomeasymptomatic before reaching adulthood



Intrinsic or nonallergic, idiosyncratic, nonatopic asthma:

Usually develops in adult age > 35 years

Non – allergic factors – respiratory infection (viral infection ismore common causative factor), physical exertion,environmental and air pollution, and occupational stimuli

Psychological and physiologic stress can also contribute to

asthmatic episodes in susceptible individuals

Acute episodes are usually more fulminant and severe thanthose of extrinsic asthma. Long-term prognosis also lessoptimistic.

Mixed asthma:

Combination of extrinsic and intrinsic asthma. Major precipitating factor is respiratory tract infection.



Status asthmaticus:

More severe clinical form

Experience wheezing, dyspnea, hypoxia

Refractory to 2 – 3 doses of β-adrenergic agents

If not managed adequately, patient may die due to

respiratory distressPrevention:

Medical history regarding

Lung diseases

Allergies to drugs, food, medication, latex

Usage of drugs, medications, natural remidies



Dialogue history:

Asthma?

Type extrinsic or intrinsic?

Age of onset

History of acute episodes

Precipitating factor

Management



Commonly prescribed drugs for the management:

Bronchodilators:

Sympathomimetic:

Albuterol

Salmeterol

Metaproterenol

Levalbuterol

Epinephrine Theophylline

Aminophylline

anticholinergic:

Ipratropium

Corticosteroids:

Beclomethasone , Triamcinolone, Flunisolide

Mometasone , Fluticasone, Budesonide

Antimediator: Cromolyn sodium, Nedocromil sodium




Stress reduction protocol in case of emotional stress

Contraindication of barbiturates and opioids as increase therisk of bronchospasm

Some inhalational anesthetics like ether irritates respiratory

mucosa

Special care should be taken while prescribing analgesics

Some patients are sensitive to bisulphites, local anesthesia iscontraindicated

Cli i l if t ti




Feeling of chest congestion

Cough, with or without sputum production

Wheezing

Dyspnea Patient wants to sit or stand up

Use of accessory muscles of respiration

Increased anxiety and apprehension

Tachypnea (>20 - >40 in severe cases)

Rise in B.P Increase in heart rate (>120 bpm in severe cases)

Only in respiratory distress Diaphoresis

Agitation

Somnolence

Confusion Cyanosis

Supraclavicular and intercostal retraction

Nasal flaring



Pathophysiology:

Neural control of airways

Airway inflammation

Immunological responses

Bronchospasm

Bronchial wall edema and hypersecretion of mucous glands

Breathing



Management:

Recognize problem (respiratory distress, wheezing)

Discontinue dental treatment

Activate office emergency team

P – Position, usually upright with arms thrown forward

A → B → C – Assess and perform basic life support as needed

D – Definitive care:Administer O2

Administer bronchodilator via inhalation

(Episode terminates) (episode continues)

Dental care may continue Activate EMSDischarge patient Administer parenteral drugs

Hospitalize or discharge patient, per EMS recommendation

Additional considerations: Sedatives which depress respiratory system and centralnervous system are absolutely contraindicated. 5mg IV or IM diazepam may be

indicated to decrease anxiety.



It is generally described as the inability of heart to supply sufficientoxygenated blood for body‟s metabolic needs.


Increase in the workload of the heart. E.g. high blood pressure

Damaging muscular walls of the heart through coronary arterydisease and myocardial infarction

e.g. Stenosis of heart valves (aortic, mitral tricuspid, pulmonary)

Increase in body‟s requirement of O2 and nutrients (e.g. pregnancy,hyperthyroidism, anemia, Paget‟s disease)

Other factors are physical, psychological and climatic stress



Prevention:

Medical history questionnaire

Dialogue history

Physical evaluation



ASA I – no dyspnea and fatigue with normal exertion. No

special dental modifications. ASA II – mild dyspnea and fatigue during exertion. Stress

reduction protocol should be considered

ASA III – dyspnea and fatigue with normal activities - Medicalconsultation, stress reduction protocol, other treatment

modifications. ASA IV – dyspnea, undue fatigue and orthopnea at all times.

Only elective procedures – dental emergencies managedwith medication – physical intervention only in hospital dentalclinics.




Heart failure –

Signs- Symptoms –

Pallor, cool skin Weakness and undue fatigue

Sweating (Diaphoresis) Dyspnea on exertion

LVH Hyperventilation Dependent edema Nocturia

Hepatomegaly and splenomegaly Paroxysmalnocturnal dyspnea

Narrow pulse pressure Wheezing (cardiac asthma)

Pulsus alterans

Ascities

A t l d



Acute pulmonary edema –

All of the signs & symptoms of heart failure

Moist rales at lungs

Tachypnea

Cyanosis

Frothy pink sputum

increased anxiety, dyspnea at rest

Pathophysiology:



Pathophysiology: Structural and functional cardiac disorder

Impairs left ventricular ability to fill with or eject blood

Limit exercise tolerance and fluid retention

Pulmonary congestion and peripheral edema

Right ventricular failure signs and symptoms related to systemic venous and capillarycongestion.

Acute pulmonary edema is a drastic symptom of heart failure

Excess fluid in alveolar spaces and interstitial tissues

Suffocation and oppression of chest

Elevates heart rate and blood pressure

Increases additional load to the heart

Further decrease in cardiac function due to hypoxia

If this vicious circle is not interrupted, it may lead rapidly to death

v

Management:

i ( i i i i i iffi i i )



Recognize problem (conscious patient exhibiting extreme difficulty in breathing)


P – Position, conscious patient in any comfortable position, usually upright


Calm the patient



Administer O2

Monitor vital signs

Alleviate symptoms of respiratory distress:

Perform bloodless phlebotomy

Administer vasodilator e. g. NitroglycerineAlleviate apprehension e.g. morphine

Discharge patient

Modify subsequent dental treatment



It is a group of diseases marked by high levels of blood glucose resultingfrom defects in insulin production, insulin action, or both


Type I diabetes:

Genetic factors

Environmental factors like drugs, toxins and viruses (mumps, rubella,coxsackie)

Autoimmune factors

Type II diabetes:

Genetic factors

Insulin secretion Insulin resistance

Obesity

Adipocyte derived hormones and cytokines

Oth ifi t f di b t llit



Other specific types of diabetes mellitus

Gestational diabetes mellitus

Impaired glucose tolerance

Impaired fasting glucose

Precipitants of hypoglycemia in diabetic patients:



Precipitants of hypoglycemia in diabetic patients:

Addison‟s disease Anorexia nervosa

Decrease in usual food intakeEthanolFactitious hypoglycemiaHepatic impairmentHyper and hypothyroidismIncrease in usual exercise

InsulinIslet cell tumorsIncorrectly used insulin pumpMalnutritionOld ageOral hypoglycemic agents

Over aggressive treatment of ketoacidosisPentamidine, Phenylbutazone, PropranololRecent change in doseSalicylatesSepsis

P ti



Prevention:


Dialogue history

Physical examinationDental therapy considerations:

ASA physical status Treatment considerations II Eat normal breakfast and take usual

insulin dose in the morning Avoid missing meals before and after

surgery If missing meal is unavoidable, consult

phycisian or ↓ insulin dose by half III Monitor blood glucose levels more

frequently for several days following

surgery and modify insulin accordingly Consider medical consultation

IV Consult physician before treatment

A tibi ti i th t i l i d i i t



Antibiotic coverage in the postsurgical period is appropriate

Stress reduction protocol to be followed

Clinical manifestations of hyperglycemia:

Symptom Type I diabetes Type II diabetes Polyuria ++ + Polydipsia ++ + Polyphagia with weightloss ++ _ Recurrent blurred vision + ++ Vulvovaginitis or pruritis + ++ Loss of strength ++ + Nocturnal enuresis ++ _ Absence of symptoms _ ++



Other symptoms of type I diabetes Other symptoms of type II diabetes Repeated skin infections Marked irritability Decreased vision Headache Paresthesias Drowsiness Loss of sensation Malaise Impotence Dry mouth Postural hypotension

Clinical manifestations of hypoglycemia:



Clinical manifestations of hypoglycemia:

Early stage – mild reaction

Diminished cerebral function

Changes in mood Decreased spontaneity

Hunger

Nausea

More severe stage Sweating

Tachycardia

Piloerection

Increased anxiety

Bizarre behavioral patterns

Belligerence

Poor judgment

Uncooperativeness

Later severe stage •Unconsciousness•Seizure activity•Hypotension•Hypothermia

Pathophysiology:



Pathophysiology:

Hyperglycemia:

Prolonged lack of insulin (type I) or prolonged lack of tissue response(type II)

Blood glucose levels remains elevated for longer time coz ofglycogenolysis and ↓ uptake by peripheral tissues

Glucose exceeds 180mg/100 ml – glucosuria

Because of its large molecular size, glucose in urine carries awaylarge volumes of water and electrolytes (Na+ & K+) – polyuria

Dehydrated state – skin dry and flushing - polydipsia Weight loss due to depletion of water, glycogen, triglyceride(TGA)

stores

Loss of muscle mass due to aminoacids → glucose and ketonebodies

TGA → free fatty acids (FFA) in the liver

FFA – acetoacetate and β – hydroxybutyrate (BHA) – diabeticketoacidosis

↓ cardiac contractility, catecholamine response, respiratoryalkalosis

Diabetic coma

Hypoglycemia:



yp g y

Hypoglycemia in adults – blood sugar < 50 mg/dl, in children -< 40 mg/dl

Alters normal functioning of the cerebral cortex

Mental confusion and lethargy

Lack of glucose → ↑ activities of sympathetic andparasympathetic nervous systems

With the mediation of epinephrine,↑ systolic and mean blood

pressures ↑ sweating and tachycardia

When the blood sugar level drops even further

Loss of consciousness

Hypoglycemic coma and insulin shock

Patients may experience tonic – clonic convulsions

Management: Hyperglycemia



Management: Hyperglycemia

Recognize problem (lack of response to sensory stimulation)



P – Position, supine position with legs elevated



Summon EMS

Establish IV infusion, 5% dextrose and water or of normal saline Administer O2

Transport to hospital

H l i i ti t



Hypoglycemia – conscious patient

Recognize problem (altered consciousness)



P – Position, patient comfotably


D – Definitive management:

Administer oral carbohydrates

If successful If unsuccessful

Permit patient to recover Activate EMSDischarge the patient Administer parenteral

carbohydrates

Monitor patient

Discharge patient

Hypoglycemia: unconscious patient



Hypoglycemia: unconscious patient

P – Position patient in supine position with feet elevated

D – Definitive management

Summon EMS

Administer oral carbohydrates

IV 50% dextrose solution

1 mg glucagon via IM or IV Transmucosal sugar, or rectal honey or syrup

Monitor vital signs every 5 minutes

Administer O2

Allow patient to recover and discharge per medical recommendations



The thyroid gland secretes three hormones (T3 T4 andcalcitonin)that are vital in the regulation of the level ofbiochemical activity of most of the body‟s tissues.


Hypothyroidism: Hyperthyroidism:



Hypothyroidism: Hyperthyroidism:

Primary: Diffuse toxic goiter

Auto immune Toxic multinodular goiter

Idiopathic causes Factitious thyrotoxicosis

Postsurgical thyroidectomy T3 thyrotoxocosis

External radiation therapy Thyrotoxicosis with thyroiditis

Radioiodine therapy Hashimoto‟s thyroiditis

Inherited enzymatic defect Subacute thyroiditis Antithyroid drugs Jod – Basedow phenomenon

Lithium, phenylbutazone Malignancies

TSH – producing tumors

Secondary:

Pituitary tumor Hypothalamic hyperthyroidism

Infiltrative disease of pituitary Struma ovarii withhyperthyroidism

Prevention:




Dialogue history

Dental therapy considerations

Euthyroid patient with normal hormone levels can bemanaged normally

Hypothyroid – avoidance of CNS depressants (opiods,sedative hypnotics)

Hyperthyroid – avoidance of atropine and vasoconstrictors,least concentrated solution is preferred 1:200,000, smallesteffective volume of anesthetic and vasodepressor, aspiration

prior to every injection

Evaluation of cardio vascular disease

Clinical manifestations



Hypothyroidism:

Symptoms Signs Paresthesias Loss of energy Intolerance to cold Muscular weakness Pain in muscles and joints Inability to concentrate Drowsiness Constipation Forgetfulness Depressed auditory acuity Emotional instability Headaches Dysarthria

Pseudomyotonic reflexes Change in menstrual pattern Hypothermia Dry, scaly skin Puffy eyelids Hoarse voice Weight gain

Dependent edema Sparse axillary and pubic hair Pallor Thinning eyebrows Yellow skin Loss of scalp hair Abdominal distension Goiter Decreased sweating

Thyrotoxicosis:



y

Symptoms signs Common Weight loss Palpitations Nervousness Tremor Less common Chest pain Dyspnea Edema Psychosis Disorientation Diarrhea Abdominal pain

Fever Tachycardia Sinus tachycardia Dysrhythmias Wide pulse pressure Tremor Thyrotoxic stare and eyelidretraction Hyperkinesis Heart failure Weakness Coma Tender liver Infiltrative ophthalmopathy Somnolence or obtundence Jaundice

Pathophysiology:



Hypothyroidism:

Insufficient levels of thyroid hormones

Body functions slow down

Infiltration of mucopolysaccharides and mucoproteins in skin

Hard nonpitting mucinous edema – myxedema

Cardiac enlargement, pericardial and pleural effusions

Cardiovascular and respiratory difficulties

End point is myxedema coma- loss of consciousness due tohypothermia, hypoglycemia and CO2 retention

Thyrotoxicosis:



Thyrotoxicosis:

Thyroid hormones ↑ body‟s energy consumption and BMR

Fatigue &weight loss

Direct actions on myocardium - ↑ HR, ↑ myocardial irritability

↑ cardiac work load

Palpitations, dyspnea, chest pain

↑ incidence of angina pectoris and heart failure

↑ thyroid hormones also affects liver function

End point – thyroid storm and crisis

M t



Management:

P – Position , supine position with feet elevated

D – Definitive management – activate EMS and if recovery is notimmediate, establish IV access

Hypothyroidism – IV doses of thyroid hormones (T3 & T4) for several days

Thyrotoxicosis – administer large doses of antithyroid drugs,additional therapy – propranolol, glucocorticoids

Administer O2

Discharge or hospitalize the patient



Defined as „any vascular injury that reduces cerebral blood flowto a specific region of the brain, causing neurologicimpairment‟. „Stroke‟, „cerebral apoplexy‟ & „brain attack‟

Classification:

cerebral ischemia and infarction – atherosclerosis &thrombosis, cerebral embolism

Intracranial hemorrhage – arterial aneurysms & hypertensivevascular disease

Others – TIA – transient ischemic attacks





Consistently elevated blood pressure is a major risk factor

Diabetes mellitus

Cardiac enlargement Hypercholesterolemia

Use of oral contraceptives

Cigarette smoking

Prevention:


Dialogue history






Length of time elapsed since the CVA – should not undergoelective dental care within 6 months of the episode

Minimization of stress – morning appointments, effective paincontrol, psychosedation during treatment

Assessment of bleeding – most of CVA patients on antiplateletor anticoagulant therapy


Common signs and symptoms – headaches, dizziness, vertigo,

drowsiness, chills, nausea, vomiting. Loss of consciousness andconvulsive movements are less common. Weakness or paralysisof extremities occurs in contralateral side. Speech defects maybe seen

Neurological signs and symptoms – paralysis of one side of body,difficulty in breathing and swallowing, inability to speak or slurring

of speech, loss of bladder and bowel control, unequal pupil size Infarction – gradual onset of signs and symptoms whereas

embolism and hemorrhage – abrupt onset of signs andsymptoms

Pathophysiology:

Cerebrovascular ischemia and Hemorrhagic CVA



Cerebrovascular ischemia and

infarction Hemorrhagic CVA

•At cellular level, ischemia •Anaerobic glycolysis withproduction of lactate •Mitochondrial dysfunction →

disruption of membrane and

vascular endothelium •BBB breaks down and edema

forms •Edema ↑ tissue mass in cranium

causes mild headache •Severe edema may forces the

portions of cerebral hemisphere

into tentorium cerebelli •Ischemia and infarction of

upperbrain stem (medulla) •Loss of consciousness and fatal

•Subarachnoid hemorrhage –

ruptured aneurysms •Intracranial hemorrhage –

hypertensive vascular disease •Once vessels rupture •Arterial blood supply fills the

cranium •↑ in intracerebral blood pressure •Rapid displacement of brain stem

into tentorium cerebelli •Ultimately death

Management of CVA & TIA:

Conscious patient



Conscious patient


P – Position patient comfortably


D – Definitive management:

Monitor vital signs

Manage signs and symptoms

If B.P elevated, semi – fowler position (450 position)

Administer O2

Do not administer CNS depressants

Symptoms resolve (TIA) Symptoms persist CVA or TIA Loss ofconsciousness

Follow up management Hospitalization P – position withfeet elevated slightly

A → B → C – Assess and perform basic life support as neededMonitor vital signs

If B.P elevated, reposition patient (slight head &chest elevation)

D definitive care: establish IV access & transport to EMT



Types:

Causes:

Congenital abnormalities

Perinatal injuries

Metabolic and toxic disorders

Head trauma

Tumors

Vascular diseases

Degenerative disorders

Infectious diseases

Partial seizures Generalized seizures Simple partial Complex partial Partial seizures evolving to generalized

tonic – clonic

Absence seizures (true petitmal) Myoclonic seizures Tonic – clonic seizures Unclassified epileptic seizures

P di i f t




Hypoxia , hypoglycemia, hypocalcemia

Flashing lights, fatigue, decreased physical health, a missedmeal, alcohol ingestion, physical or emotional stress, sleepand menstrual cycle

Prevention:

Care in selection of LA agent & use of proper technique Medical history questionnaire about fainting spells, seizures

Dialogue history about previous experience of seizures, onset,duration, management


Conscious sedation – N2O – O2 & benzodiazepines




Simple partial seizure – individual remains conscious while alimb jerks for several seconds

Complex partial seizures – altered consciousness with alteredbehavioral patterns (automatisms) like some uncoordinatedpurposeless activities (lip smacking, chewing or sucking)

Absence seizure – sudden immobility and a blank stare andminor facial clonic movements

Tonic- clonic seizure –



preictal phase: ↑in anxiety and depression , appearance of auraand soon loses consciousness, a series of myoclonic jerksoccur (epileptic cry)

↑ HR, B.P, bladder pressure, piloerection, glandular hypersecretion, mydriasis, apnea

Ictal phase: series of generalized skeletal muscle contractionsprogresses to a extensor rigidity of extremities and trunk – tonic component

Generalized clonic movements, heavy stertorous breathing,alternate muscle relaxation and violent flexor contractions –

clonic component

Postictal phase: tonic – clonic movements cease, breathingreturns to normal, consciousness gradually returns

Pathophysiology:



Intrinsic intracellular and extracellular metabolic disturbances inneurons of epileptic patients

Excessive and prolonged depolarisation

↑ in neuronal permeability to sod. And pot. Ions

Ach. & GABA sustained membrane depolarization followed bylocal hyper polarization

This abnormal discharge propagated through neuronalpathways and partial seizure becomes generalized

Management of petitmal seizures:



P – position patient with feet elevated

Seizure ceases: reassure patient seizure continues (> 5 min)

Allow patient to recover before discharge A → B → C – Assess and perform BLS

Management of tonic clonic seizure:

Prodromal phase



Prodromal phase


Ictal phase


Activation of EMS


D – Definitive care

Protect patient from injury

Post ictal phase



D – Definitive care

Administer O2

Monitor vital signs

Reassure patient and permit recovery

Discharge patient

To hospital To home To physician



Signs and Symptoms of Epinephrine Toxicity

Agitation, weakness, and headache.

Pallor, tremor, palpitation.

Sharp rise in blood pressure and heart rate.

Signs and Symptoms of Local Anesthetic Toxicity

Agitation.

Muscular twitching and tremors.

Increased blood pressure and heart rate.

Light-headedness. Visual and auditory disturbances (Tinnitis, Difficulty focussing.)

If moderate to high overdose of Local anesthetic can also haveconvulsions and depression of blood pressure, heart rate, andrespiration.

MANAGEMENT OF TOXIC REACTIONS TO EPINEPHRINE:



Toxic effect of epinephrine is transitory rarely lasting morethan a few minutes

Stop dental treatment.

Place patient in most comfortable position.


Consider administering oxygen.

Allow time for the patient to recover.

Dental Treatment Considerations for use of Epinephrine

Due to its cardiovascular effects limit use in patients withhistory of heart disease or stroke.

Can cause uterine contractions in the pregnant female.

Possible drug interactions (Especially MAO inhibitors andCocaine.)

Remember the patient has endogenous epinephrineproduction of this is increased in stressful situations.

MANAGEMENT OF TOXIC REACTIONS TO LOCAL ANESTHETIC: treatment varies with the onset and severity of the reaction.



y

MILD REACTION/RAPID ONSET (Example is an intravascular

injection) Reassure patient.

Administer Oxygen.

Monitor and record vital signs.

Allow for recovery; determine if patient can be allowed toleave unescorted.

MILD REACTION/SLOW ONSET

Toxic reaction with a delayed onset is most likely a result of

impaired biotransformation. Evolves slowly, use caution.

Monitor patient, record vital signs.

SEVERE OVERDOSE/RAPID ONSET, SEVERE OVERDOSE/SLOW ONSET

ABC‟s



ABC s.

Activate EMS.

Administer Oxygen by mask at 10-15L/minute.

Start IV if available (18 gauge catheter with Normal Saline.)

If needed and available administer anticonvulsant, Versed(Midazolam)

2mg, then 1mg/min to effect (Monitor respiration.)

Monitor and record vital signs.

Allow for recovery and discharge with appropriate escort or transport to hospital if required.

Treatment Considerations to Avoid Adverse Drug Reaction

Prevention is the key. Take a complete medical history.



Prevention is the key. Take a complete medical history.Determine if there are any diseases present that affect the useof a drug.

Know what medications the patient is taking and possible drug

interactions. Careful injections make sure to aspirate to avoid an

intravascular injection.

Maximum Recommended Doses of Local Anesthetic

Lidocaine “Plain” 4.4mg/kg Lidocaine 2% with 1:100k Epinephrine 7.0mg/kg

Mepivicaine “Plain” 4.4mg/kg

Mepivicaine with 1:20k Neocobefrine 6.6mg/kg

Bupivicaine with 1:200k Epinephrine 3.2mg/kg

Maximum Recommended Doses of Epinephrine

Healthy Adult 0.2mg

Cardiac Patient 0.04mg



Signs and Symptoms of an Allergic Reaction

Cutaneous reactions are the most common occurrence andinclude urticarial, exanthematous, and eczemoid reactions.Itching is common and can also find exfoliative dermatitisand bullous dermatosis.

Angioedema (Swelling) this varies from localized slightswelling of the lips, eyelids, and face to more uncomfortableswelling of the mouth, throat, and extremities.



Respiratory (Tightness in chest, sneezing, bronchospasm)

bronchospasm is a generalized contraction of bronchialsmooth muscles resulting in the restriction of airflow. This mayalso be accompanied by edema of the bronchiolar mucosa.Bronchospasm is more common with pre-existing pulmonarydisease such as asthma or infection but can also be caused

by the inhalation of a foreign substance.

Ocular reactions include conjunctivitis and watering of eyes.

Hypotension can occur with any allergic reaction.

Anaphylaxis:



Signs and symptoms include:

Cardiovascular shock including; pallor, syncope, palpitations,tachycardia, hypotension, arrythmias, and convulsions.

Respiratory symptoms include; sneezing, cough, wheezing,

tightness in chest, bronchospasm, laryngospasm.

Skin is warm and flushed with itching, urticaria, andangioedema.

Nausea, vomiting, abdominal cramps, and diarrhea alsopossible.



Evaluation of Allergic Reactions: Things to remember.

Skin manifestations may precede more seriouscardiorespiratory problems.

Recognition of skin reactions and early treatment may abortmore serious problems.

Most important factor is assessing the seriousness of thecondition is the rate of onset.

Reactions that occur greater than one hour after theadministration of the allergen will usually be of a non-emergent nature.

TREATMENT



General Treatment

ABC‟s

Maintain airway, administer oxygen, and determine possible need for intubation or surgical airway.


If in shock put patient in a horizontal or slight Trendelenburg position.

Mild Reactions

Antihistamines usually effective. (Benadryl 50-100mg or Cholpheniramine maleate 4-12 mg IV, or IM.)

Identify and remove allergen.

Follow up medications in 4-6 hours.

Severe Reactions

If available start IV Fluids Epinephrine is drug of choice. Usually prepackaged 1:1,000 in 1mg vials

or syringe

If IV in place titrate 1:1,000 solution to effect.

If drop in blood pressure is minimal, start with 0.5ml (0.5mg.)

If drop in blood pressure is severe start with 2ml (2mg.)

Repeat after 2 minutes if needed.



If no IV use 1:1,000 (1mg/CC) IM 0.3 to 0.5mg (0.3-0.5CC.)

For an adult repeat this dose in 10 to 20 minutes.

If the patient is intubated can give epinephrine endotracheally If Asthma, edema, or pruritis (Itching) are present can use

Corticosteroids. However these drugs are to slow acting to beused for an emergency situation.

Hydrocortisone sodium succinate (Solu-cortef) 100-500mg IV or IM. Dexamethasone (Decadron) 4-12mg IV or IM.

Repeat dose at 1, 3, 6, and 10 hours as indicated by severity ofsymptoms.

Other Considerations

Monitor and record vital signs. Seizures are possible as a result of circulatory or respiratory

insufficiency.

Most severe allergic reactions require hospitalization andobservation for 24 hours.



Defined as „ a characteristic thoracic pain, usually substernal,

precipitated chiefly by exercise, emotion, or a heavy meal;relieved by vasodilator drugs, and a few minutes rest; and aresult of a moderate inadequacy of the coronary circulation‟

Precipitating factors:

Physical activity

Hot, humid environment Cold whether

Large meals

Emotional stress

Caffeine ingestion

Fever, anemia, thyrotoxicosis Cigarette smoking

Smog

High altitudes

Second – hand smoke

Types:



Types:

Stable (classic or exertional)

Variant (prinzmetal , vasospastic)

Unstable (crescendo, acute coronary insufficiency)

Prevention:

Medical history questionnaire – chest pain, shortness ofbreath, history of heart disease, stroke, high B.P, family historyof diabetes & heart problems, thyroid and diabetes, previoussurgeries and medications

Dialogue history – type of pain, radiation, precipitatingfactors and effect of nitro glycerine


Avoid overstressing the patient



g p

Supplemental oxygen via nasal cannula or nasal hood duringthe treatment – 3-5 L/min

Pain control during therapy – appropriate use of localanesthesia – smaller dose with maximum effect – slowadministration

Vasodepressor administration should be minimized inincreased risk patients

Psychosedation – N2O – O2 is preferable

Monitoring vital signs

Nitroglycerine premedication 5 min before treatment


Pain: sudden onset of chest pain described as a sensation of



Pain: sudden onset of chest pain, described as a sensation ofsqueezing, burning, pressing, choking, aching, bursting,tightness or gas

Dull aching heavy pain located substernally

Radiation of pain: most commonly to left shoulder and arm(ulnar nerve distribution)

Less frequently to right shoulder, arm, left jaw, neck andepigastrium

Pathophysiology:

Imbalance between myocardial oxygen demand and supply



y yg pp y

Compensatory mechanism by coronary arteries

If myocardial oxygen requirement reaches this critical level

Myocardial ischemia

Clinical manifestation of angina pain due to adenosine ,bradykinin, histamine and serotonin from ischemic cells

If there is consistent high B.P and tachycardia → ↑work load of

the heart

Ventricular dysrhythmias and becomes fatal

Management: Recognize problem (chest pain – angina attack)



Discontinue dental treatmentActivate office emergency team

P – Position, patient comfortably usually upright

A → B → C – Assess and perform BLS

D – definitive management

HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINAAdminister vasodilator and O2 Activate EMS

Transmucosal nitroglycerine spray O2 and consider nitroglycerineOr sublingual nitroglycerine tablet Monitor and record

0.3 – 0.6 mg for every 5 min (3 doses)

IF PAIN RESOLVES IF PAIN DOES NOT RESOLVEFuture dental treatment modifications Activate EMS

Administer aspirinMonitor and record vital signs

Medical management of unstable angina – Nitrates, β – blockers, calciumchannel blockers and psychological stress management and

reassurance



It is a clinical syndrome caused by a deficient coronary arterialblood supply to a region of myocardium that results in cellular death and necrosis


Atherosclerosis and coronary artery disease Coronary thrombosis, occlusion and spasm

Other risk factors are-

Males

5th and 6th decades of life

Undue stress

Location of infarction:



Prevention:

M di l hi t ti i h t i h t f



Medical history questionnaire – chest pain, shortness ofbreath, history of heart disease, stroke, high B.P, family history

of diabetes & heart problems, thyroid and diabetes, previoussurgeries and medications

Dialogue history – episodes of angina, last myocardialinfarction and currently taking medications

Vital signs should be recorded before and immediately after dental appointments

Visual examination – peripheral cyanosis, coolness of

extremities, peripheral edema, possible orthopnea


Avoid overstressing the patient



Supplemental oxygen via nasal cannula or nasal hood duringthe treatment – 3-5 L/min and 5 – 7 L/min

Pain control during therapy – appropriate use of localanesthesia – smaller dose with maximum effect – slowadministration

Vasodepressor administration is a relative contraindication

Psychosedation – N2O – O2 is preferable

It is strongly recommended that elective dental care isavoided until at least 6months after MI

Medical consultation and anticoagulation and antiplatelettherapy need not be altered

Inferior alveolar NB and Posterior superior alveolar NB – risk ofhemorrhage – should be avoided




Symptoms Signs Pain – severe to intolerable Prolonged, 30 min Crushing, choking Retrosternal Radiates – left arm, hand,

epigastrium, shoulders,neck, jaw Nausea and vomiting Weakness Dizziness Palpitations

Cold perspiration Sense of impending doom

Restlessness Acute distress Skin – cool, pale, moist Heart rate – bradycardia

to tachycardia; PVC

(premature ventricularcontractions) common

Pathophysiology:

Infarction of myocardium



Left ventricle is commonly involved in acute MI

Blood supply leaving the heart may be diminished

Signs and symptoms of acute MI

Larger the infarct, greater the circulatory insuficiency

Signs and symptoms of heart failure

Increased left ventricular pressure

Left ventricular failure → hypotension, ↓ cardiac output, cardiogenicshock

Fatal

Management: Recognize problem (chest pain – no history of angina)




Discontinue dental treatmentActivate office emergency team

P – Position, patient comfortably usually upright

A → B → C – Assess and perform BLS

D – definitive management

HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINAFollow protocol of angina (presumptive

diagnosis: Acute MI)Activate EMS

Administer O2,consider nitroglycerine

Administer aspirinManage pain (parenteral

opioids, N2O – O2)Monitor and record vital signs

Prepare to manage complications (suddencardiac arrest)Transfer to emergency department



Prompt recognition and efficient management of medicalemergencies by a well-prepared dental team can increasethe likelihood of a satisfactory outcome. The basic algorithmfor managing medical emergencies is designed to ensurethat the patient‟s brain receives a constant supply of bloodcontaining oxygen.

References

Caroline, Nancy L., Emergency Medicine in the Streets,2nd Ed 1983 Little and Brown



2nd Ed., 1983, Little and Brown. Malamed, Stanley, Managing Medical Emergencies,

Journal of the American Dental Association, Vol. 124,pp40-59, August 1993.

Malamed, Stanley, Emergency Medicine: Beyond theBasics, Journal of the American Dental Association, Vol.128, pp843-854, July 1997.

Malamed, Stanley, Medical Emergencies in the Dental

Office, 4th

Ed. 1993, Mosby. Prusinski, L., Fundamentals of Corticosteroid Therapy, Oral

Medicine Department, Nation Naval Dental Center,Bethesda, MD, 1997.

Walker, H.K., Hall, W.D., Hurst, J.W., Clinical Methods, TheHistory, Physical, and Laboratory Examinations, 2nd Ed.,

1980, Butterworths. Whitehouse, Michael, Medical Emergencies for Dental

Officers, 2nd Dental Battalion/Naval Dental Center, CampLejeune, NC, 1998.

Sem 2 Medical Emergencies Dental Office

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